Serum lipid profile of polycystic ovary syndrome in Sudanese women

Transcription

1 Research Article Serum lipid profile of polycystic ovary syndrome in Sudanese women Abstract Omer Mohamed Shoaib 1, Saadalnour Mohamed Mustafa 2, Ihab Hamed Nourein 3 1 Department of Clinical Chemistry, Faculty of Medical Laboratory Sciences, Alzaeim Alazhari University, Sudan. 2 Department of Histopathology and Cytology, Faculty of Medical Laboratories Sciences, Al-Neelain University, Sudan. 3 Department of Pathology, Najran University, Najran, Saudi Arabia. Correspondence to: Omer Mohamed Shoaib, oshoaib13@yahoo.com Received April 19, Accepted May 18, 2015 Background: Polycystic ovarian syndrome (PCOS) has been one of the major public health problems in Sudan, which leads to medical consequences. It is caused by several factors such as menstrual dysfunction, hyperandrogenism, hirsutism, dyslipidemia, and obesity, which elevate the risk of diabetes mellitus and cardiovascular disease. Objective: To know the lipid profile variation in Sudanese women with PCOS. Materials and Methods: This descriptive, analytic, cross-sectional, and hospital-based study was conducted in Khartoum state, Sudan; it was carried out from March 2013 to May 2014.The subjects enrolled for the study included 200 women with PCOS who were compared with 100 healthy women of the control group; all of them were age and weight matched. Samples were taken after overnight fasting, and then serum lipid levels were analyzed using enzymatic colorimetric methods. Data management and analysis were done by using Microsoft Excel and SPSS software, version Result: The mean age of patients with PCOS was ± 5.4 years, and the mean age of subjects in the control group was ± 4.93 years. Lipid profile parameters in PCOS group were as follows: the (mean ± SD) of serum triglyceride, total cholesterol, high-density lipoprotein (HDL), and low-density lipoprotein (LDL) were ± mg/dl, ± mg/dl, ± mg/dl, and ± mg/dl, respectively, while those of control group were ± mg/dl, ± mg/dl, ± mg/dl, and ± mg/dl, respectively. There were statistically significant increased levels of triglyceride, total cholesterol, and LDL cholesterol (LDL-C) in PCOS group when compared with the control group (P < 0.05) and decreased level of HDL cholesterol (HDL-C). Conclusion: The altered lipid profile in PCOS patients showed a sign of cardiovascular disease. KEY WORDS: Polycystic ovary syndrome, triglyceride, total cholesterol, HDL-C, LDL-C Introduction Polycystic ovary syndrome (PCOS) is the most common endocrine disease and metabolic disorder in adolescent and reproductive women, which is the predominant reason for female infertility, with the incidence in 5% 10% of women of Website: DOI: /ijmsph Access this article online Quick Response Code: reproductive age. [1,2] Chronic anovulation, hyperandrogenism, and ovarian polycystic changes observed by ultrasound examination in clinic are the conditions, which confirm the prevalence of PCOS. Although the causative factors of PCOS are not well known, previous studies have shown the close association of PCOS with lipid metabolism disorder and insulin resistance. [3,4] Over 50% of patients with PCOS showed obesity (android-type), which indicated an elevated risk of diabetes mellitus and cardiovascular disease (CVD). [5] Approximately 40% 50% of patients, especially obese women, exhibit insulin resistance. [6] The PCOS that entitles a unique attention was first described in 1935 by Stein and Leventhal, and this condition is also known as polycentric ovaries, sclerocystic ovarian disease, Stein Leventhal syndrome, chronic anovulatoy syndrome, and polycystic ovarian disease (PCOD). [7] Earlier, the clinical diagnosis was based on International Journal of Medical Science and Public Health Online Omer Mohamed Shoaib. This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 International License ( allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material for any purpose, even commercially, provided the original work is properly cited and states its license. 1605

2 the trio of hirsutism, amenorrhea, and obesity. The diagnosis of PCOS is based on the Rotterdam criteria for the presence of any two of the following conditions: (i) chronic anovulation, (ii) clinical/biochemical parameters for hyperandrogenism, and (iii) polycystic ovaries on ultrasonography. [8] Insulin resistance, hyperandrogenism, and dyslipidemia are presumed to be the major risk factors for CVD in women with PCOS. [9,10] Insulin resistance and dyslipidemia allegedly play a key role on the risk of cardiovascular pathology in women with PCOS. The extent to which dyslipidemia leads to this risk is still not well understood. [11] Dyslipidemia is the most common abnormality in PCOS, [12] with elevated levels of total cholesterol, triglycerides (TGs), and low-density lipoprotein cholesterol (LDL-C) and with low levels of high-density lipoprotein cholesterol (HDL-C). [5,13] Talbott et al. [14] reported increased level of LDL-C in patients with PCOS, and Conway et al. [15] reported that the most characteristic lipid alteration is decreased levels of HDL-C. There are few studies done to know the alteration in serum lipid profile in PCOS patients; thus, this study was done to know the lipid profile variation in women with PCOS. Materials and Methods This descriptive, analytic, cross-sectional, and hospitalbased study was carried out in educational hospital of Khartoum state, Sudan, from March 2013 to May 2014; all patients selected showed a history of PCOS. Subjects enrolled for the study included 200 patients diagnosed with PCOS and 100 healthy women (control group) who showedno history of drugs affecting lipid metabolism (with normal menstrual cycle and sex hormone level and no evidence of polycystic ovary). A written informed consent was obtained from all the participants; all of them were age and weight matched. The blood samples were obtained to determine the levels of lipids parameters. The blood samples were drawn after overnight fasting in the morning (between 8 a.m. and 11 a.m.). Blood samples of 5 ml from each individual of the study population were collected from both cases and control. The blood samples were centrifuged at 3,000 rpm for 10 min and sera obtained; samples were stored in +4 C until analyzed during the same day. Enzymatic colorimetric methods were used to determine total cholesterol, TGs, HDL-C, and LDL-C levels. All these parameters were investigated and recorded, and then, a comparison was made between PCOS patients and control participants. Later, the results were collected and presented in graphs and tables, showing the values as mean ± standard deviation. Data were analyzed by SPSS, version 20 (IBM). Student t-test was used for the calculation. P 0.05 was considered significant. All the chemical reagents were purchased from Bio Systems company (Spine Company for analytical material and chemical reagents). Result A total of 200 patients with PCOS were included in the study with a mean age of ± 5.41 years and 100 healthy women with a mean age of 31.23±4.93 years. Other basic characteristics of the study participates such as body mass index (BMI) of the PCOS patients was statistically significantly increased when compared with control group [Table 1]. The mean ± SD of the lipid profile parameters in PCOS group of serum TG, total cholesterol, HDL, and LDL were ± mg/dl, ± mg/dl, ± mg/dl, and ± mg/dl, respectively, while those of control group were ± mg/dl, ± mg/dl, ± mg/dl, and ± mg/dl, respectively [Table 2]. There were statistically significant increased levels of TG, total cholesterol, and LDL-C in PCOS group and decreased levels of HDL-C when compared with the control group (P < 0.05) [Table 2]. In our study, the correlations between BMI and all the parameters in the study were found. Figure 1 shows no correlation between BMI and the serum levels of TGs (r = 0.00, P = 0.001). Figure 2 shows insignificant and very weak positive correlation between BMI and the serum levels of cholesterol (r = 0.04, p = 0.55). Figure 3 shows insignificant, very weak positive correlation between BMI and the serum levels of HDL (r = 0.01, P = 0. 84). Figure 4 shows insignificant, very weak positive correlation between BMI and the serum levels of LDL (r = 0.04, P = 0. 56). Table 1: Mean ± SD of baseline characteristics of patients with PCOS and control group Variable PCOS group Control group P Age (years) ± ± Weight (kg) ± ± Height (cm) ± ± Height (cm) ± ± P < 0.05 is statistically significant. Table 2: Mean ± SD of lipid parameters in the PCOS group and control group Parameters PCOS group Control group P Serum triglyceride (mg/dl) ± ± Serum cholesterol (mg/dl) ± ± Serum HDL-C (mg/dl) ± ± Serum LDL-C (mg/dl) ± ± P < 0.05 is statistically significant. 1606

3 Figure 1: A scatter plot showing the correlation between body mass index (BMI) and triglycerides in the study group (r = 0.00). Figure 2: A scatter plot showing the correlation between body mass index (BMI) and cholesterol in the study group (r = 0.04, P = 0.55). 1607

4 Figure 3: A scatter plot showing the correlation between body mass index (BMI) and high density lipoproteins (HDL) in the study group (r = 0.01, P = 0.84). Figure 4: A scatter plot showing the correlation between body mass index (BMI) and low density lipoproteins (LDL) in the study group (r = 0.04, P = 0.56). 1608

5 Discussion The study was conducted to evaluate the changes in lipid profile parameters in Sudanese PCOS patients and healthy women as control group. PCOS is one of the important endocrine disorders causing reproductive abnormalities in women, which has heterogeneous clinical features and multifactorial etiology. [16] Dyslipedemia is one of the important risk factors associated with PCOS. Obesity and insulin resistance occur frequently in association with this syndrome. Cardiovascular risk factors seem to cluster in women with PCOS when compared with general population. [17] In our study, levels of total cholesterol, TG, and LDL-C were statistically higher, and level of HDL-C was lower in PCOS patients, when compared with age-matched healthy females [Table 2]. This is similar to the results observed in PCOS patients in another study. [18] Moreover, similar results found by some studies suggest that PCOS patients were hyperlipidemic with higher total cholesterol, LDL-C, and TGs concentrations and lower HDL-C levels than control [19,20] On the other hand, our results were not concurrent with the study done by Bickerton et al. [21] who demonstrated that there were no significant differences in lipid or lipoprotein concentrations between patients with PCOS and weight-matched controls. Lipid abnormalities were closely related to insulin resistance independent of obesity. [22] The increase in TGs may be because of the accumulation of TGs, which may occur owing to the increased lipogenesis, decreased clearance, or reduced oxidation of fatty acids. Increased secretion of very-low-density lipoprotein (VLDL) particles by the liver resulted in elevated plasma TGs concentration. This may occur because of insulin resistance, which is seen in PCOS patients. Insulin resistance also contributes more catabolism of HDL-C particles and formation of LDL-C. [23] Hyperandrogenism also contributed for altered lipid profile. Hyperandrogenism has been associated with increased hepatic lipase activity and has a role in the catabolism of HDL-C particles. Increased serum concentrations of TGs have also been recognized as a risk factor for CVD. [24] Our study showed that there was no correlation between the BMI and the serum TGs [Figure 1]. Moreover, in our study, the serum level of HDL-C was significantly decreased in the subjects in the PCOS group [Table 2] (P < 0.05). Similar results were found in study done by Wild et al. [25] They found that women with PCOS showed lower HDL-C levels, higher LDL/HDL ratios, and higher TG levels than regularly menstruating women. More recently, Slowinska-Srzednicka et al. [26] have drawn the attention to the role of insulin in the lipid abnormalities observed in hyperandrogenic women with PCOS. These investigators compared 27 women with PCOS with 22 eumenorrheic control subjects stratified by weight (obese and nonobese). Women with PCOS showed significantly lower levels of HDL 2 and higher levels of apob and TGs. Our study, demonstrated that women with PCOS showed higher significant increase in the serum levels of LDL-C when compared with the control subjects; similar results were found by Pirwany [27] On the other hand, this study showed an insignificant correlation between the BMI and the serum levels of LDL [Figure 2]. This agreed with the results of a study done by Pirwany [27] who concluded that women with PCOS show increased hepatic lipase activity and LDL relative to BMImatched controls with normal menstrual rhythm and normal ovaries. Furthermore, these metabolic disturbances appeared to be related more closely to abnormal insulin metabolism and circulating androgen levels. Our study showed that women with PCOS showed significantly decreased serum levels of HDL-C [Table 1] when compared with the control subjects; this result was similar to the study done by Wild et al. [25] in 1985 who found that women with PCOS showed lower serum levels of HDL-C in comparison with healthy control subjects. Recently, Slowinska-Srzednicka et al. [26] have drawn the attention to the role of insulin in the lipid abnormalities observed in hyperandrogenic women with PCOS, when they compared 27 women with PCOS with 22 eumenorrheic control subjects stratified by weight (obese and nonobese); they found that women with PCOS showed significantly lower levels of HDL and an insignificant correlation between the BMI and the serum levels of HDL [Figure 3]. Finally, in our study, there was a significant increased serum level of total cholesterol when compared with the control subjects and an insignificant correlation between the BMI and the serum levels of total cholesterol [Figure 2] Conclusion From this study, it is concluded that women with PCOS have altered lipid profile, with higher levels of (TGs, total cholesterol, and LDL) and low level of serum HDL; this difference may play a role in the pathophysiology found in women with PCOS. Further studies are needed to clarify the role of lipids in these women. Moreover, elevated serum lipids reflected the metabolic state in those patients; all patients should be screened for dyslipidemia for effective cardiovascular risk prevention. References 1. Adams J, Polson DW, Franks S. Prevalence of polycystic ovaries in women with anovulation and idiopathic hirsutism. Br Med J (Clin Res Ed) 1986;293(6543): Car BR. Williams s Textbook of Endocrinology, 8th edn. Philadelphia, PA: WB Saunders, pp Galluzzo A, Amato MC, Giordano C. Insulin resistance and polycystic ovary syndrome. Nutr Metabol Cardiovasc Dis 2008;18(7): Teede HJ, Hutchison S, Zoungas S, Meyer C. Insulin resistance, the metabolic syndrome, diabetes, and cardiovascular disease risk in women with PCOS. Endocrine 2006;30(1): Wild RA. Obesity, lipids, cardiovascular risk, and androgen excess. Am J Med 1995;98(Suppl 1A):S

6 6. Aral SO, Cates W Jr. The increasing concern with infertility. Why now? JAMA 1983;250(17): Morrell V. Basic fertility assessment. Prim Care 1998;24: Saxena P, Prakash A, Nigam A, Mishra A. Polycystic ovary syndrome: is obesity a sine qua non? A clinical, hormonal, and metabolic assessment in relation to body mass index. Indian J Endocrinol Metab 2012;16(6): Mohamadin AM, Habib FA, Al-Saggaf AA. Cardiovascular disease markers in women with polycystic ovary syndrome with emphasis on asymmetric dimethylarginine and homocysteine. Ann Saudi Med 2010;30(4): Gonzalez F, Rote NS, Minium J, Kirwan JP. Evidence of proatherogenic inflammation in polycystic ovary syndrome. Metabolism 2009;58(7): Pepe I, Agrusa A, Rinella MR, Fertita E, Gulotta P, Scozzari F, et al. Heterogenous forms of dyslipidemia in women with polycystic ovary syndrome. Acta Medica Mediterranea 2008;24: Legro RS, Kunselman AR, Dunaif A. Prevalence and predictors of dyslipidemia in women with polycystic ovary syndrome. Am J Med 2001;111(8): Dahlgren E 1, Johansson S, Lindstedt G, Knutsson F, Odén A, Janson PO, et al. Women with polycystic ovary syndrome wedge resected in 1956 to 1965: a long-term follow-up focusing on natural history and circulating hormones. Fertil Steril 1992;57(3): Talbott E, Clerici A, Berga SL, Kuller L, Guzick D, Detre K, et al. Adverse lipid and coronary heart disease risk profiles in young women with polycystic ovary syndrome, results of a case control study. J Clin Epidemiol 1998;51(5): Conway GS, Agrawal R, Betteridge DJ, Jacobs HS. Risk factors for coronary artery diseases in lean and obese women with the polycystic ovary syndrome. Clin Endrocrinol (Oxf) 1992;37(2): Zawadic JK, Danif A. Diagnostic criteria for polycystic ovarian syndrome: towards a rational approach. In: Polycystic Ovary Syndrome, Dunaif A, Givens JR, Haseltine F (Eds.). Cambridge, England: Blackwell Science,1992. pp Wlid RA. Long-term health consequences of PCOS. Hum Reprod Update 2002;8(3): Valkenburg O, Steegers-Theunissen RP, Smedts HP, Dallinga- Thie GM, Fauser BC, Westerveld EH, et al. A more atherogenic serum lipoprotein profile is present in women with polycystic ovary syndrome: a case-control study. J Clin Endocrinol Metab 2008;93(2): Meirow D, Raz I, Yossepowitch O, Brzezinski A, Rosler A, Schenker JG, et al. Dyslipidaemia in polycystic ovarian syndrome: different groups, different aetiologies? Hum Reprod 1996;11(9): Orio F Jr, Palomba S, Spineli L, Cascella T, Tauchmanova L, Zullo F, et al. The cardiovascular risk of young women with polycystic ovary syndrome: an observational, analytical prospective case-control study. J Clin Endocrinol Metab 2004; 89(8): Bickerton AST, Clark N, Meeking D, Shaw KM, Crook M, Lumb P, et al. Cardiovascular risk in women with polycystic ovarian syndrome (PCOS). J Clin Pathol 2005;58(2): S. Tangvarasittichai, Poonsub P, Tangvarasittichai O. Association of serum lipoprotein ratios with insulin resistance in type 2 diabetes mellitus. Indian J Med Res 2010;131(5): Saxena P, Prakash A, Nigam A. Efficacy of 2-hour post glucose insulin levels in predicting insulin resistance in polycystic ovarian syndrome with infertility. J Human Reprod Sci 2011;4(1): St-Onge MP, Janssen I, Heymsfield SB. Metabolic syndrome in normal-weight Americans: new definition of the metabolically obese, normal-weight individual. Diabetes Care 2004;27(9): Wild RA, Painter PC, Coulson PB, Carruth KB, Ranney GB. Lipoprotein lipid concentrations and cardiovascular risk in women with polycystic ovary syndrome. J Clin Endocrinol Metab 1985;61(5): Slowinska-Srzednicka J, Zgliczynski S, Wierzbicki M, Srzednicki M, Stopinska-Gluszak U, Zgliczynski W, et al. The role of hyperinsulinemia in the development of lipid disturbances in nonobese and obese women with the polycystic ovary syndrome. J Endocrinol Invest 1991;14(7): Pirwany I. Obstetrics and Gynecology. 2009; How to cite this article: Shoaib OM, Mustafa SM, Nourein IH. Serum lipid profile of polycystic ovary syndrome in Sudanese women. Int J Med Sci Public Health 2015;4: Source of Support: Nil, Conflict of Interest: None declared. 1610